Yoshiyama K O, Kimura S
a Department of Bioresource and Environmental Sciences , Kyoto Sangyo University , Kyoto , Japan.
c Department of Molecular and Chemical Life Sciences , Tohoku University , Sendai , Japan.
Plant Signal Behav. 2018;13(6):e1477904. doi: 10.1080/15592324.2018.1477904. Epub 2018 Jun 25.
The DNA damage response system (DDR) is crucial in addressing DNA double-strand breaks (DSBs), which pose a severe threat to genomic integrity. The SOG1 transcription factor is a master regulator of the Arabidopsis thaliana DDR. We previously showed that hyperphosphorylation of five Ser-Gln sites of SOG1 is the molecular switch to activate the DDR. In this study, we determined that SOG1 is hyperphosphorylated within 20 minutes following DSB-inducing treatment, followed by activation of several SOG1 target genes. Using SOG1 phosphorylation mutants, we demonstrated that although the hyperphosphorylation sites remain unchanged over time, the amount of hyperphosphorylation gradually increases. These observations suggest that rapid SOG1 hyperphosphorylation is limited by the amount of active kinases.
SOG1, suppressor of gamma response; ATM, Ataxia telangiectasia mutated; ATR, ATM and Rad3-related.
DNA损伤反应系统（DDR）在应对DNA双链断裂（DSB）方面至关重要，DNA双链断裂对基因组完整性构成严重威胁。SOG1转录因子是拟南芥DDR的主要调节因子。我们之前表明，SOG1五个丝氨酸-谷氨酰胺位点的过度磷酸化是激活DDR的分子开关。在本研究中，我们确定在诱导DSB的处理后20分钟内SOG1发生过度磷酸化，随后几个SOG1靶基因被激活。使用SOG1磷酸化突变体，我们证明尽管过度磷酸化位点随时间保持不变，但过度磷酸化的量逐渐增加。这些观察结果表明，快速的SOG1过度磷酸化受活性激酶量的限制。
SOG1，γ反应抑制因子；ATM，共济失调毛细血管扩张突变蛋白；ATR，ATM和Rad3相关蛋白 。
